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Post-concussion syndrome is symptoms that can linger following a concussion. Studies have shown cannabis reduces damage caused from brain injuries and can help patients manage the symptoms of the syndrome.
Overview of Post-Concussion Syndrome
Post-concussion syndrome (PCS) is a variety of symptoms, including headaches and dizziness, that continue for weeks and sometimes months following a concussion. A concussion is a mild traumatic brain injury that typically occurs after a direct blow to the head. Not all concussions lead to post-concussion syndrome, which doesn’t seem to be correlated to the severity of the initial blow.
What causes post-concussion symptoms to develop following certain concussions is yet to be identified. According to Mayo Clinic, some experts believe the symptoms come from structural damage to the brain or the disruption of neurotransmitter systems. Others believe that psychological factors may contribute.
In addition to headaches and dizziness, post-concussion syndrome commonly causes fatigue, irritability, anxiety, insomnia, loss of concentration and memory, and noise and light sensitivity.
Typically, symptoms associated with PCS develop within the first seven to 10 days after a concussion and eventually alleviate within a three-month period. In some cases, however, the symptoms can persist for a year or longer.
Treatment for post-concussion syndrome depends on individual symptoms. Headaches are commonly treated with medications. Time, however, is often the best therapy for treating memory and thinking problems.
Findings: Effects of Cannabis on Post-Concussion Syndrome
While research on cannabis’ direct effect on post-concussion syndrome is lacking, preclinical findings have shown that cannabis offers therapeutic benefits following brain injuries. Studies have shown that the cannabinoids found in cannabis interact with the body’s cannabinoid receptors (CB1 and CB2). These receptors are part of the endocannabinoid system, and they provide protection against neural damage following acute and chronic brain damage (Lopez-Rodriguez, et al., 2013).
For example, in one study, the administration of cannabinoids following a traumatic brain injury decreased brain swelling and inflammation and was shown to improve recovery (Shohami, et al., 2011). Others have showed that cannabinoids, through the activation of the endocannabinoid system, prevent glutamate excitotoxicity, intracellular calcium accumulation, activation of cell death pathways, microglia activation, neurovascular reactivity and circulating leukocytes following a brain injury. Researchers have suggested that modulating the endocannabinoid system could be an effective way to provide neuroprotection and prevent and reduce brain injury (Abush & Akirav, 2013) (Arain, Khan, Craig & Nakanishi, 2015) (Lopez-Rodriguez, et al., 2013) (Panikashvili, et al., 2006) (Shohami, et al., 2011).
Studies have also shown that cannabis can help post-concussion syndrome patients manage the symptoms associated with the disorder. Cannabis can lower stress, help combat depression, improve sleep and reduce pain (Abush & Akirav, 2013) (Wilsey, et al., 2013).
States That Have Approved Medical Marijuana for Post-Concussion Syndrome
Currently, only the state of Illinois has approved medical marijuana for the treatment of post-concussion syndrome. However, in Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment. In addition, a number of other states will consider allowing medical marijuana to be used for the treatment of post-concussion syndrome with the recommendation from a physician. These states include: California (any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), Rhode Island (other conditions subject to approval), and Washington (any “terminal or debilitating condition”).
Also, fourteen states have approved medical marijuana specifically to treat “chronic pain,” which can develop from post-concussion syndrome. These states include: Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island, Vermont and West Virginia. The states of Nevada, New Hampshire, North Dakota, Ohio and Vermont allow medical marijuana to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania, Washington and West Virginia have approved cannabis for the treatment of “intractable pain.”
Recent Studies on Cannabis’ Effect on Post-Concussion Syndrome
- Abush, H., & Akirav, I. (2013). Cannabinoids Ameliorate Impairments Induced by Chronic Stress to Synaptic Plasticity and Short-Term Memory. Neuropsychopharmacology, 38(8), 1521–1534. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682147/.
- Arain, M., Khan, M., Craig, L., and Nakanishi, S.T. (2015, March). Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Annals of Clinical and Translational Neurology, 2(3), 289-94. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369278/.
- Donat, C.K., Fischer, F., Walter, B., Deuther-Conrado, W., Brodhun, M., Bauer, R.., and Brust, P. (2014). Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet. Acta Neurobiologiae Experimentalis, 74,197-210. Retrieved from http://www.ane.pl/linkout.php?pii=7419.
- López Rodríguez, A.B., Mateos Vicente, B., Romero-Zerbo, S.Y., Rodriguez-Rodriguez, N., Bellini, M.J., Rodriguez de Fonseca, F., Bermudez-Silva, F.J., Azcoitia, I., Garcia-Segura, L.M., and Viveros, M.P. (2011, September). Estradiol decreases cortical reactive astrogliosis after brain injury by a mechanism involving cannabinoid receptors. Cerebral Cortex, 21(9), 2046-55. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bhq277.
- Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202.
- Nguyen, B.M., Kim, D., Bricker, S., Bongard, F., Neville, A., Putnam, B., Smith J., and Plurad, D. (2014, October). Effect of marijuana use on outcomes in traumatic brain injury. The American Surgeon, 80(10), 979-83. Retrieved from http://www.ingentaconnect.com/content/sesc/tas/2014/00000080/00000010/art00015.
- Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V., Kohen, R., Alexandrovich, A., and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease, 22(2), 257-74. Retrieved from http://www.sciencedirect.com/science/article/pii/S0969996105003074.
- Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from http://www.nature.com/nature/journal/v413/n6855/full/413527a0.html.
- Post-concussion syndrome. (2014, August 19). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/post-concussion-syndrome/basics/definition/con-20032705.
- Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., & Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/.
- Wilsey, B., Marcotte, T., Deutsch, R., Gouaux, B., Sakai, S., and Donaghe, H. (2013, February). Low-dose vaporized cannabis significantly improves neuropathic pain. The Journal of Pain, 14(2), 136-48. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566631/.
- Xu, Z., Lv, X.A., Dai, Q., Ge, Y.Q., and Xu, J. (2016). Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI. Molecular Brain, 9, 75. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971620/.